Mafa expression enhances glucose-responsive insulin secretion in neonatal rat beta cells.

ABSTRACT:

Aim/hypothesis

Neonatal beta cells lack glucose-stimulated insulin secretion and are thus functionally immature. We hypothesised that this lack of glucose responsiveness results from a generalised low expression of genes characteristic of mature functional beta cells. Important glucose-responsive transcription factors, Mafa and Pdx1, regulate genes involved in insulin synthesis and secretion, and have been implicated in late beta cell development. The aim of this study was to assess whether Mafa and/or Pdx1 regulates the postnatal functional maturation of beta cells.

Methods

By quantitative PCR we evaluated expression of these and other beta cell genes over the first month compared with adult. After infection with adenovirus expressing MAFA, Pdx1 or green fluorescent protein

SUBMITTER: Aguayo-Mazzucato C 

PROVIDER: S-EPMC3047400 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature